KLK3: tumorigenic or not?

We have just published our latest review about the role of KLK3 as an activator of VEGF-C and VEGF-D in prostate cancer. Prostate cancer is one of the most common cancers in males. It is not a question whether you will get it but only when.

 Once you reach your 80s, the likelihood of you having prostate cancer is bigger than not having it. In a , who died of other causes, 59% of those older than 80 had prostate cancer. It is likely that many of these cases were indolent, and never would have caused any problems. Only a few of them might have become synptomatic had these men lived longer. 

So there is a significant interest in distinguishing those cancers that are going to cause problems. Many prognostic markers have been proposed to do exactly that: to predict which cancers would become problematic.

From the vascular biology point of view, angiogenesis and lymphangiogenesis are two hallmarks of cancers that have been previously proposed to have prognostic value. , we thought that this might have significance for prostate cancer. Meanwhile, further research has clarified some questions and it really seems to be that both VEGF-C and VEGF-D are involved in cancer progression. it is not clear yet which proteases are responsible for the activation of VEGF-C and VEGF-D in real human cancers. KLK3- or Cathepsin D (CTSD)-activated VEGF-D might be one behind the resistance of tumors to bevacizumab (Avastin) treatment. The consequences of VEGF-C activation, on the other hand, are more difficult to predict, because actiavted VEGF-C does simulataneously both good and bad: It facilitates metastasis, but on the other hand allows for a enhanced immune response against the tumor. Interesting research lies ahead. Read more in our review: